Contributors: Shay Brikman conceived the work and wrote the draft. Veronika Denysova, Husam Menzal and Guy Dori analyzed and interpreted the data and revised the manuscript critically for important intellectual content. All of the authors gave final approval of the version to be published and agreed to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

When chest symptoms recur in a patient who underwent percutaneous transluminal coronary angioplasty (PTCA), it is necessary to rule out restenosis (R). Three main noninvasive tests suggest the presence of R: exercise stress test (XT), myocardial perfusion imaging (MPI) and stress echocardiography (s-echo). The objectives of this review were: (1) to estimate the pretest probability of R as a function of time after PTCA in symptomatic patients and (2) to obtain an approximation of the diagnostic parameters of the XT, MPI and s-echo for detecting R. A MEDLINE search (English-language, years: 1980-2001) was conducted to identify studies examining post-PTCA functional testing for diagnosing R. Data from the studies were pooled. Comparing studies was often difficult due to varying methodology in the studies. Pretest probability of R in symptomatic patients increases in a nonlinear fashion from 20% or less at 1 month, to nearly 90% at 1-year postangioplasty. The approximated accuracy of the XT, MPI, and s-echo for detecting R was 62, 82 and 84%, respectively. During the first month after PTCA, none of the noninvasive modalities is able to accurately detect R. Late (7-9 months) after PTCA, the pretest probability of R is high and therefore the noninvasive measure may be spared. Our analysis suggests that MPI and s-echo should be preferred over the XT for diagnosing R.

Hepatic encephalopathy and myxedema coma share clinical features: coma, ascites, anemia, impaired liver functions, and a "metabolic" electroencephalogram (EEG). Hyperammonemia, a hallmark of hepatic encephalopathy, has also been described in hypothyroidism. Differentiation between the 2 conditions, recognition of their possible coexistence, and the consequent therapeutic implications are of utmost importance. We describe a case of an 82-year-old woman with a history of mild chronic liver disease who presented with hyperammonemic coma unresponsive to conventional therapy. Further investigation disclosed severe hypothyroidism. Thyroid hormone replacement resulted in gain of consciousness and normalization of hyperammonemia. In patients with an elevated ammonia level, altered mental status, and liver disease, who do not have a clear inciting event for liver disease decompensation, overwhelming evidence of hepatic decompensation, or who do not respond to appropriate therapy for hepatic encephalopathy, hypothyroidism should be considered and evaluated.